AUTOIMMUNITEIT BIJ COPD

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable lung disease, characterised by a progressive, not fully reversible airflow limitation and associated with an immunerespons, mucus hypersecretion and/or destruction of alveolar wall, leading to emphysema. Tobacco smoke is the main risk factor in western countries for the pathogenesis of COPD, up to 80-90% of all patients is or was a smoker. Even after smoking cessasation the decline in lungfunction continues, although not as rapidly as when the patient continues smoking. Still, only 10-20% of all smokers develops COPD. The inflammatory reaction and a loss of self-tolerance and in the lungs of COPD patients suggest a parallel with autoimmune diseases. It is known that lungs of COPD patients contain more neutrophils and macrophages than lungs of healthy controls. Also, previous studies showed a higher number of oligoclonal B lymphocytes, sometimes organised in lymphoid follicles, in the lungs and airways of COPD patients. Finally, autoantibodies directed against, for instance, airway epithelial cells, endothelial cells and elastin, were found in a considerable number of COPD patients. These results however were never confirmed. The hypothesis of this study is that patients with different stages of COPD possess circulating autoantibodies directed against lungtissue and/or –components, while healthy controls possess little to no. Data and serum of COPD patients and smoking, ex-smoking and non-smoking healthy controls were collected for this study. The antibody binding of IgA and IgG to an epithelial lung cell-line (A549) and a fibroblast lung cell-line (MRC-5) was determined with a ELISA. The binding to non-treated A549 cells and 10% cigarette smoke extract (CSE) treated A549 cells was visualized by immunohistochemical stainings. The ELISA data did not show significant differences in IgA and IgG binding to the A549 and MRC-5 lung cell-lines between COPD patients and healthy controls. Nevertheless, there was a clear individual variation, which was also seen in the immunohistochemical stainings of non-treated and CSE treated A549 cells. Additionally the IgG staining of CSE treated cells was, in contrast to what was expected, more intense in the control group. The COPD group however had a significantly higher rate of strongly positive pixels, which suggests a more specific binding. This research shows that binding of circulating IgA and IgG to lung cell-lines is possible, but there were no convincing differences between COPD patients and healthy controls. With these results we can neither confirm nor refute that autoimmunity plays a role in the pathogenesis of COPD. Yet it can be stated that there are clear individual differences and that autoimmunity may play a role, along with other risk factors, in the pathogenesis of COPD in a specific group of patients.